Ayman El-Menyar (Doha / QA), Mohammad Asim (Doha / QA), Naushad Ahmad Khan (Doha / QA), Hassan Al-Thani (Doha / QA), Sandro Rizoli (Doha / QA)
Background: We investigated the impact of early beta-blockers (BB) administration on the adrenergic surge, inflammatory cytokines, and traumatic brain injury (TBI) biomarkers based on high sensitivity troponin T (HsTnT) status in TBI patients with varying severities.
Methods: This is ongoing prospective, randomized, controlled, double-blind trial (BBTBBT). Patients were stratified based on the severity of the head injury and HsTnT status prior to randomization. Patients with positive HsTnT received propranolol (group-1; n=110), and those with negative HsTnT were randomized to receive either propranolol (group-2; n=129) or placebo (group-3; n=111). Luminex and ELISA-based immunoassays were used to quantify the serum levels of inflammatory cytokines, TBI biomarkers (S100B and enolase) and epinephrine.
Results: A total of 350 blunt TBI adult patients were enrolled. Group-1 had higher baseline levels of IL-6 &1B, S100B, lactate, and base deficit compared to the randomized groups (p=0.001). The baseline IL-18 &8, enolase, and epinephrine levels were not significantly different between the studied groups. Group-1 showed temporal reduction in IL-6, IL-1B, epinephrine, and enolase levels from baseline to 48 h post-injury (P=0.001). Patients with severe head injuries had substantially higher baseline levels of IL-6, IL-1B, S100B, HsTnT, and CRP as compared with mild or moderate head injuries (P=0.01). However, baseline levels of IL-8 &18, epinephrine, and Enolase did not differ significantly between the three groups.
Conclusion: Early BB administration showed a significant reduction in cytokine levels and TBI biomarkers from baseline to 48 h post-injury, particularly in patients with positive troponin, indicating its potential role in controlling inflammation in TBI. The elevated levels of IL-6, IL-1B, S100B, and HsTnT were associated with severe TBIs. These findings highlight the potential role of BBs in modulating inflammation-mediated immune responses in TBI patients.
none to declare
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